As the elderly comprise an ever greater proportion of the population, peripheral vascular disease becomes an increasingly significant problem. Although the mechanisms of plaque formation are being investigated extensively, very little research has involved study of the mechanisms of physiological compensation to occlusion of veins or arteries. Since no method has evolved to prevent the occlusions, perhaps more research should be directed toward an understanding of normal compensatory mechanisms so that they may be assisted by external intervention. The response of the peripheral vasculature to chronic venous distention will be evaluated by determining changes in resistance in the large artery, small vessel, and venous segments of the vascular tree resulting from chronic venous occlusion. The role of the sympathetic nervous system in the changes in vascular function will be determined by observing the change in resistance following gamma-receptor blockade. The rate of anatomical changes of the venous wall in the altered vascular function will be evaluated by direct measurements of resting venous volume and venous distensibility. Alterations in the size, numbers and patterns of veins and competence of valves will be evaluated from casts of the vasculature. All results will be compared to a paired normal extremity. The effectiveness of various therapeutic procedures in stimulating collateral development following arterial occlusion will be evaluated in rats from 1) claudication times, 2) pressure differentials across the collateral bed and 3) anatomic resistance as determined from vascular casts.